title: [Effects of pyrrolidine dithiocarbamate on expressions of α-smooth muscle actin, integrin α5 and fibronectin in acute paraquat poisoned rats].
abstract: OBJECTIVE
  To observe the expressions of α-SMA, integrin α5 and fibronectin (Fn) in acute paraquat poisoned rats and the effect of PDTC. To investigate the mechanism of paraquat-induced pulmonary fibrosis.
  
  
  METHODS
  Sprague-Dawley rats were randomly divided into three experimental groups: Control group (6 rats), PQ group (36 rats) and PQ+PDTC group (36 rats). On the 1st, 3rd, the 7th, the 14th, the 28th and the 56th day after exposure, the protein expression of α smooth muscle actin (α-SMA) was evaluated by western blot. The mRNA levels of integrin α5 and fibronectin (Fn) were analyzed with real-time quantitative PCR (RT-PCR). Meanwhile, the lung pathological changes were observed and semi-quantified.
  
  
  RESULTS
  T With the time passing, the expression of α-SMA in PQ group increased gradually compared with control group (P < 0.05 or P < 0.01). The increasing extent was gently on the 3 rd, the 7 th day. While increasing extent was rapidly from the 28 th to the 56 th day. RT-PCR showed PQ significantly increased Fn mRNA level on all time points and increased integrin α5 mRNA level from the 7 rd to 56 th day compared with control group (P < 0.05 or P < 0.01). PDTC treatment significantly deceased α-SMA, Fn, and integrin α5 levels compared with PQ group in corresponding time points (P < 0.05 or P < 0.01) Noteworthy, in PQ+PDTC group, the occurrence of pathological changes were drastically attenuated and pathologic score significantly decreased (P < 0.05 or P < 0.01).
  
  
  CONCLUSIONS
  α-SMA, integrin α5 and fibronectin could play an important role in the development of pulmonary fibrosis caused by paraquat poisoning. PDTC, asa strong NF-κB inhibitor, may inhibit NF-κB activity and further significantly decreased expressions of α-SMA, integrin α5 and fibronectin which were important part of ECM, leading to drastically attenuated pulmonary fibrosis. However, the mechanisms of PDTC intervention still remains to be explored.
authors.affiliation: School of Public Health, Ningxia Medical University, Yinchuan 750004, China.
authors.forename: Min
authors.initials: M
authors.lastname: Huang
authors.forename: Hui-fang
authors.initials: HF
authors.lastname: Yang
authors.forename: Ping
authors.initials: P
authors.lastname: Zhang
authors.forename: Xiu-li
authors.initials: XL
authors.lastname: Chang
authors.forename: Zhi-jun
authors.initials: ZJ
authors.lastname: Zhou
mesh_terms: D000199:Actins / Q000378:metabolism*; D000818:Animals; D004195:Disease Models, Animal; D005353:Fibronectins / Q000378:metabolism*; D039482:Integrin alpha5 / Q000378:metabolism*; D008297:Male; D010269:Paraquat / Q000506:poisoning*; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000378:metabolism*; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013859:Thiocarbamates / Q000494:pharmacology*
chemical_list: D000199:Actins; D005353:Fibronectins; D039482:Integrin alpha5; D010269:Paraquat; D011759:Pyrrolidines; D013859:Thiocarbamates; C498862:Acta2 protein, rat; C020972:pyrrolidine dithiocarbamic acid